Mos is not required for the initiation of meiotic maturation in Xenopus oocytes
Mos is not required for the initiation of meiotic maturation in Xenopus oocytes
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DOI：
10.1093/emboj/cdf400
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发表时间：
2002-08-01
期刊：
影响因子：
11.4
通讯作者：
Haccard, O
中科院分区：
文献类型：
--
作者：
Dupré, A;Jessus, C;Haccard, O
在非洲爪蟾卵母细胞中，c-mos原癌基因产物已被提出作用于孕酮的下游，以控制进入减数分裂I，从减数分裂I到减数分裂II的过渡，其特征在于没有S期，以及在受精前观察到的中期II停滞。在这里，我们报告说，抑制莫斯合成的吗啉代反义寡核苷酸不阻止胆甾酮诱导的启动非洲爪蟾卵母细胞减数分裂成熟，如以前认为的。Mos-depleted卵母细胞完成减数分裂I，但未能在中期II停止，进入一系列胚胎样细胞周期，伴随着Cdc 2活性和DNA复制的振荡。我们提出，独特的和保守的作用Mos是阻止有丝分裂细胞周期的雌性配子，直到受精在非洲爪蟾，海星和小鼠卵母细胞。
In Xenopus oocytes, the c-mos proto-oncogene product has been proposed to act downstream of progesterone to control the entry into meiosis I, the transition from meiosis I to meiosis II, which is characterized by the absence of S phase, and the metaphase II arrest seen prior to fertilization. Here, we report that inhibition of Mos synthesis by morpholino antisense oligonucleotides does not prevent the progesterone-induced initiation of Xenopus oocyte meiotic maturation, as previously thought. Mos-depleted oocytes complete meiosis I but fail to arrest at metaphase II, entering a series of embryonic-like cell cycles accompanied by oscillations of Cdc2 activity and DNA replication. We propose that the unique and conserved role of Mos is to prevent mitotic cell cycles of the female gamete until the fertilization in Xenopus, starfish and mouse oocytes.